VOL. 1, NO. 1, July 2013
International Journal of Health and Medical Sciences
©2012-2013. All rights reserved.
http://www.ejournalofhealth.org/
Periodontal Abscess: A Review
1
Dr. Anarthe Raju Yadav, 2 Dr. Ameet Madan Mani, 3 Dr. P.P. Marawar
1
: Sr. Lecturer, 2-Reader, 3-Prof & Head Dept. of Periodontology Rural Dental College,
Pravara Institute of Medical Sciences, Loni-413736 Tal : Rahata Dist Ahmednagar, Maharashtra (India)
1
[email protected]
ABSTRACT
Periodontal abscess is the third most frequent dental emergency, representing 7–14% of all the dental emergencies.
Numerous etiologies have been implicated: exacerbations of the existing disease, post-therapy abscesses, the impaction of
foreign objects, the factors altering root morphology etc. The diagnosis is done after analysis of the signs and symptoms
and by the using supplemental diagnostic aids. Evidences suggest that the micro flora which are related to periodontal
abscesses are not specific and that they are usually dominated by gram negative anaerobe, rods etc. The treatment of the
periodontal abscess has been a challenge for many years. Today three therapeutic approaches are being discussed in
dentistry that include, drainage and debridement, systemic antibiotics and periodontal surgical procedures which are
applied in the chronic phase of the disease. Antibiotics like Penicillin, Metronidazole, Tetracyclines and Clindamycin are
the drugs of choice. This review focuses on the classification, etiology and clinical characteristics of periodontal abscesses
and its management in the clinical practice.
Keywords: Periodontal abscess, incision and drainage, antibiotics, periodontal surgery.
1. INTRODUCTION
Periodontal Abscess is a localized purulent
infection in the periodontal pocket that may lead to the
destruction of periodontal ligament and alveolar bone.
The international conference on research in the biology of
periodontal disease in 1977 defined a periodontal abscess
as, “an acute, destructive process in the periodontium
resulting in localized collection of pus communicating
with oral cavity through the gingival sulcus or other
periodontal sites and not arising from the tooth pulp.”[1]
The important characteristics of the periodontal abscess
include: a localized accumulation of pus in the gingival
wall of the periodontal pockets; usually occurring on the
lateral aspect of the tooth; the appearance of edematous
red and shiny gingiva; may have a dome like appearance
or may come to a distinct point. These conditions have to
be promptly managed, failure of which could lead to loss
of teeth and danger of cellulitis in susceptible patients.
Depending on the nature and course of the periodontal
abscess an immediate attention is required to relieve pain
and systemic complications. Moreover, the presence of an
abscess may also modify the prognosis of the involved
tooth and in many cases, may be responsible for
extraction of tooth. Therefore accurate diagnosis and the
immediate treatment of the abscess is an important step in
the management of periodontal abscess.
a.
b.
c.
d.
e.
2. ETIOLOGY OF PERIODONTAL
ABSCESS
The etiology of periodontal abscess is at times
difficult to determine basically due to the size of the
abscess, the possible condition that can result in a purulent
infection and the vast number of potentially infective
microbiota present.
f.
Tortuous
periodontal
pocket
especially
associated with furcation defects. These can
eventually become isolated and can favor
formation of an abscess.
Closure of margins of periodontal pocket may
lead to extension of the infection into the
surrounding supporting periodontal tissue due to
the pressure of the suppuration inside the
obstructed periodontal pocket. Fibrin secretions,
leading to the local accumulation of pus may
favor the closure of gingival margin to the tooth
surface. [2]
Changes in composition of the micro flora,
bacterial virulence or defect in host defense
could also make the pocket lumen inefficient to
drain the increased suppuration . [3]
After procedures like scaling and root planning
where calculus is dislodged and pushed into the
soft periodontal tissue. It may also be due to
inadequate scaling which will allow calculus to
remain in the deepest periodontal pocket area
while the resolution of the inflammation at the
coronal pocket area will occlude the normal
drainage and entrapment of the sub gingival flora
in the deepest part of the pocket which cause
abscess formation. [4]
Treatment with systemic antibiotics without sub
gingival debridement in patients with advanced
periodontitis leads to a change in the
composition of the sub gingival microbiota
leading to super infection and abscess formation .
[5]
As a consequence of perforation of the lateral
wall of a tooth by an endodontic instrument
during root canal therapy. [6]
Following are the sum of factors causing
periodontal abscess.
13
VOL. 1, NO. 1, July 2013
International Journal of Health and Medical Sciences
©2012-2013. All rights reserved.
http://www.ejournalofhealth.org/
Prevotella intermedia- 25-100% [9]
Porphyromonas gingivalis-55-100% [10]
Fusobacterium nucleatum -44-65% [12]
Actinobacillus
actinomycetemcomitans-25%
[11], [12]
Camphylobacter rectus- 80% [12]
Prevotella melaninogenica-22% [12]
3. CLASSIFICATION OF PERIODONTAL
ABSCESS [7]
3.1 Based on Etiological Criteria
a. Periodontitis related abscess: When acute
infections originate from a biofilm in the
deepened periodontal pocket.
b. Non-Periodontitis related abscess: When the
acute infections originate from other local
source. eg. Foreign body impaction, alteration in
root integrity.
3.2 Based on the Course of the Disease
a. Acute periodontal abscess: The abscess
develops in a short period of time and lasts for a
few days or weeks. An acute abscess often
presents as a sudden onset of pain on biting and a
deep throbbing pain in a tooth in which the
patient has been tending to clench. Associated
lymph node enlargement may be present.
b.
Chronic periodontal abscess: This is the
condition that lasts for a long time and often
develop slowly. In The chronic stages a nasty
taste and spontaneous bleeding may accompany
discomfort. The adjacent tooth is tender to bite
on and is sometimes loose. Pus may be present as
also may be discharges from the gingival crevice
or from a sinus in the mucosa overlying the
affected root. Pain is usually of low intensity.
Occasionally the abscess may already be
draining through one or more sinus tracts into the
oral cavity. Often regional lympadenopathy and
occasionally slight elevation of body temperature
may also associated due to abscess.
4. MICROBOLOGY OF PERIODONTAL
ABSCESS
a.
b.
c.
d.
e.
f.
g.
Bacteroids
melaninogenicus
subspecies,
Fusobacterium subspecies, Vibrio corroders,
Capnocytophaga species, Peptococcus species
and Peptostreptococcus species.[1]
Purulent oral infections are polymicrobial and
usually caused by endogenous bacteria, however
very few studies have investigated the specific
microbiota of periodontal abscesses [8].
About 60% of cultured bacteria were strict
anaerobes [9].
Most frequent type of bacteria was gram
negative anaerobic rods and gram positive
facultative cocci.
In general, gram negatives predominated over
gram positive and rods over cocci [10].
Reports showed that high percentage of
abscesses harbor lactamase producing bacteria
[11]
Culture studies of periodontal abscesses have
revealed high prevalence of the following
bacteria:
5. PATHOGENESIS
After the infiltration of pathogenic bacteria to the
periodontium, the bacteria and or bacterial products
initiate the inflammatory process consequently activating
the inflammatory response. Tissue destruction is caused
by the inflammatory cells and their extracellular enzymes.
An inflammatory infiltrate is formed, followed by the
destruction of the connective tissue. The encapsulation of
the bacterial mass occur and pus formation takes place.
The lowered tissue resistance and the virulence as well as
the number of bacteria present determine the course of
infection. The entry of bacteria into the soft tissue wall
initiates the formation of the periodontal abscess.
6. INVESTIGATIONS FOR
PERIODONTAL ABSCESS
6.1 Radiographs
Dental radiographs (periapical, bitewings and
OPG), Gutta percha point placed through sinus might
locate the source of the abscess.
6.2 Pulp Vitality Test
Thermal or electrical tests to assess the vitality
of the tooth.
6.3 Microbial Test
Sample of pus from the sinus, abscess or
pruluent material expressed from the gingival crevice
could be sent for culture and sensitivity test.
6.4 Others
Assessment of diabetic status through blood
glucose and glycosylated hemoglobin.
7. GUIDELINES
FOR
PROGNOSIS [13]
a.
b.
c.
d.
e.
ASSESSING
Horizontal mobility more than 1mm.
Class II-III furcation involvement of multirooted
tooth.
Probing pocket depth > 8 mm.
Poor response to periodontal therapy.
More than 40% alveolar bone loss.
8. DIAGNOSIS
ABSCESS
OF
PERIODONTAL
A periodontal abscess is diagnosed on the basis
of chief complaints and history of present illness. Usually,
the severity of the pain and distress will differentiate an
acute from a chronic abscess. The relevant medical and
dental history is mandatory for the proper diagnosis of
such cases.
14
VOL. 1, NO. 1, July 2013
International Journal of Health and Medical Sciences
©2012-2013. All rights reserved.
http://www.ejournalofhealth.org/
The important point to be considered while
taking the history includes:
a. Whether the patient is under the care of a
physician or a dentist
b. Whether the patient is presently on any
medication or whether he/she has any medical
condition that may affect the periodontal
diagnosis and treatment.
c. Any previous dental treatment that may affect
the diagnosis or the treatment plan
d. The history of smoking is important because
heavy smokers can develop a more severe
periodontal disease and they do not respond very
well to periodontal therapy.
9. DIFFERENTIAL
DIAGNOSIS
PERIODONTAL ABSCESS
OF
9.1 Gingival Abscess
A localized purulent infection that involves the
marginal gingiva or interdental papilla. Features that
differentiate the gingival abscess from the periodontal
abscess are:
i. History of recent trauma;
ii. Localisation to the gingiva;
iii. No periodontal pocketing
9.2 Periapical Abscess
Inflammatory condition characterized by
formation of purulent exudate involving the dental pulp or
pulpal remnants and the tissues surrounding the apex of a
tooth.
Periapical abscess can be differentiated by the
following features:
i. Located over the root apex
ii. Non-vital tooth, heavily restored or large filling
iii. Large caries with pulpal involvement.
iv. History of sensitivity to hot and cold food
v. No signs / symptoms of periodontal diseases.
vi. Periapical radiolucency on intraoral radiographs.
9.3 Perio-Endo lesion
The Perio-endo lesion usually shows:
i. Severe periodontal disease which may involve the
furcation
i. Severe bone loss close to the apex, causing
pulpal infection
ii. Non-vital tooth which is sound or minimally
restored
9.4 Endo-Perio lesion
Endo-perio lesion can be differentiated by:
i. Pulp infection spreading via the lateral canals
into the perodontal pockets.
ii. Tooth usually non-vital, with periapical
radiolucency
iii. Localised deep pocketing
9.5 Cracked tooth Syndrome
Cracked tooth Syndrome can be differentiated by:
i. History of pain on mastication
ii. Crack line noted on the crown.
iii. Vital tooth
iv. Pain upon release after biting on cotton roll,
rubber disc or tooth sleuth
v. No relief of pain after endodontic treatment
9.6 Root fracture
Root fracture can be differentiated by the
presence of following characteristics.
i. Heavily restored crown
ii. Non-vital tooth with mobility
iii. Post crown with threaded post
iv. Possible fracture line and radiolucency around
the root which are visible in periapical
radiographs
v. Localised deep pocketing, normally one site only
vi. Might need an open flap exploration to confirm
diagnosis
10. TREATMENT
ABSCESS
OF
PERIODONTAL
The principles of management of periodontal
abscess are as follows:
1. Local measures
a. Drainage
b. Eliminate cause
2. Systemic measures: Antibiotics in conjunction with
local measures
The management of a patient with periodontal abscess
can divided into three stages:
• Immediate management
• Initial management
• Definitive therapy
10.1 Immediate Management [14]
a. In life threatening infections, hospitalization,
supportive therapy together with antimicrobial
therapy will be necessary.
b. Depending on the severity of the infection and
local signs and symptoms the clinical
examination, investigations and initial therapy
can be delayed.
c. In non life threatening conditions systemic
measures such as oral analgesics and
antimicrobial chemotherapy will be sufficient to
eliminate systemic symptoms, severe trismus and
diffuse spreading infection (facial cellulites).
d. Antibiotics are prescribed empirically after
microbiological
analysis
and
antibiotic
sensitivity of pus and tissue specimen.
e. The empirical regimens are dependent on the
severity of the infection. The common antibiotics
used are
15
VOL. 1, NO. 1, July 2013
International Journal of Health and Medical Sciences
©2012-2013. All rights reserved.
http://www.ejournalofhealth.org/
Phenoxymethyle penicillin 250 -500 mg qid 5-7 days
Amoxycillin 250 - 500 mg tds 5-7 days
Metronidazole 200 - 400 mg tds 5-7 days
If allergic to penicillin
Erythromycin 250 –500 mg qid 5-7 days
Doxycyline 100mg bd 7-14 days
Clindamycin 150-300 mg qid 5-7 days
defenses (radiation therapy and axillary
dissection). A periodontal abscess was associated
with the development of a cervical necrotizing
fasciitis. A necrotizing cavernositis was thought
to be related to a severe periodontal infection,
including three periodontal abscesses.
11. SUMMARY
10.2 Initial Management:
a. Irrigation of abscessed pocket with saline or
antiseptics [15)]
b. Removal of foreign bodies [16)]
c. Drainage through sulcus with a probe or light
scaling of tooth surface [17)]
d. Compression and debridement of soft tissue wall
[17)]
e. Oral hygiene instructions
f. Review after 24-48 hours.
Alternative Treatments [17)]
3. Extraction of teeth with hopeless prognosis
10.3 Definitive Therapy
Definitive treatment following reassessment after
initial therapy has to perform to restore, function, esthetics
of periodontium & to enable patient maintain periodontal
health. Gingivectomy or periodontal flap surgery with
systemic antibiotics or local antibiotics (tetracycline) is
indicated as definitive treatment of perioodntal abcess
[18].
10.3.1 Complications of Periodontal Abscess:[19]
a. Tooth loss: Periodontal abscesses have been
suggested as the main cause for tooth extraction
during the phase of supportive periodontal
therapy (SPT). A tooth with a history of repeated
abscess formation is considered to be a tooth
with a questionable prognosis. In a retrospective
study, 45% of teeth with periodontal abscesses in
a SPT population were extracted.
b.
Dissemination of the infection: A number of
publications, mainly case reports, have described
different systemic infections in different parts of
the body, in which the suspected source of
infection was a periodontal abscess.
Two possible sources of dissemination have been
described:
• Dissemination of the bacteria inside the tissues
during therapy. A case of pulmonary
actinomycosis was related to the treatment of a
periodontal abscess, which was ultrasonically
scaled 1 month earlier. A case of brain abscess
was observed in a healthy patient with a
periodontal abscess who was treated with
drainage and curettage without systemic
antibiotic 2 weeks earlier.
• Bacterial dissemination through the blood
stream due to bacteremia from an untreated
abscess. Cellulitis in breast cancer patients have
been reported following gingivitis or an abscess,
due to transient bacteremia and reduced host
In spite of their long historical recognition,
periodontal abscess after present challenge in terms of
diagnosis, etiology, treatment and prognosis. The
periodontal abscess is the 3rd most frequent dental
emergency and it is especially prevalent among untreated
periodontal patients and periodontal patients during
maintenance. Different etiologies have been proposed,
and two main groups can be distinguished, depending on
its relation with periodontal pockets. In the case of a
periodontitis related abscess, the condition may appear as
an exacerbation of a non-treated periodontitis or during
the course of periodontal therapy. In non-periodontitis
related abscesses, impaction of foreign objects and
ridiculer abnormalities are the two major causes. The
abscess micro flora seems to be similar to that of adult
periodontitis and it is dominated by gram negative
anaerobic rods, including well known periodontal
pathogens. Complications and consequences include tooth
loss and the spread of the infection to other body sites.
Diagnosis and treatment is mainly based on empiricism,
review; microbiology; diagnosis; classification; etiology;
prevalence.
REFERENCES
[1]
Robert J Genco, Henry M Goldman, D Walter
Cohen, Contemporary Periodontics; 6th Edition;
1980: Page 476-482
[2]
Carranza FJ. Glickman’s Clinical Period ontology.
7th Edition; 1990: Page 259-265, Philadelphia: WB,
Saunders Company.
[3]
Dewitt GV, Cobb CM & Killoy WJ; The acute
periodontal abscess: Microbial penetration of tissue
wall. ;Int. J Periodontics & Restorative Dentistry
1985: 39:51
[4]
Kareha MJ, Rosenberg Es & De Haven H;
Therapeutic considerations in the management of a
periodontal abscess with an intrabony defect.;
Journal of Clinical Period ontology; 1981: 8; 375386.
[5]
Dello Russo MM; The post-prophylaxis
periodontal abscess: etiology and treatment.
International Journal of Periodontics and
Restorative Dentistry; 1985: 29-37.
[6]
Helovuo H, Hakkarainen K & Paunio K; Changes
in the prevalence of sub gingival enteric rods,
staphylococci and yeasts after treatment with
penicillin and erythromycin. Oral Microbiology
and Immunology; 1985: 8; 75-79.
16
VOL. 1, NO. 1, July 2013
International Journal of Health and Medical Sciences
©2012-2013. All rights reserved.
http://www.ejournalofhealth.org/
[7]
Herrera D, Rolda´n S, Sanz M; The periodontal
abscess: a review J Clin Periodontol; 200: 27: 377–
386.
[8]
Tabaqhali S; Anaerobic infections in the head and
neck region. Scandinavian Journal of Infectious
Diseases; 1988: 57; 24-34.
[9]
Topoll HH, Lange DE & Muller RF; Multiple
periodontal abscesses after systemic antibiotic
therapy. Journal of Clinical Period ontology; 1990:
17; 268-272.
[10]
Newman MG & Sims TN; The predominant
cultivable microbiota of the periodontal abscess
Journal of Period ontology; 1979: 50; 350-354.
[11]
Lewis MAO, Parkhurst CL, Douglas CW, martin
MV, Absi EG, Bishpo PA, Jons SA.; Prevalence of
penicillin resistant bacteria in acute suppurative
oral
infection.
Journal
of Antimicrobial
Chemotherapy; 1995: 35, 785-791.
[12]
Hafstrom CA, Wikstrom MB, Renvert SN &
Dahlen G; Effect of treatment on some
periodontopathogens and their antibody levels in
periodontal abscesses. Journal of Period ontology;
1994: 65; 1022-1028
[13]
Schwartz M, Lamster IB; Clinical guide to
periodontics. 1985 : WB Saunders pp.
[14]
Ahl DR, Hilgeman JL & Snyder JD; Periodontal
emergencies. Dental Clinics of North America
;1986: 30, 459-472
[15]
Abrams H & Kopezyk RA; Gingival sequelae from
a retained piece of dental floss. Journal of the
American Dental Association; 1983: 106, Page 5778.
[16]
Ammons KJ; Lesion in the oral mucous
membranes. Acute lesions of the periodontium.
Fundamentals of Periodontics. Eds. Wilson T &
Korman K.; 1996: Page 435-440. Singapore:
Quintessence.
[17]
Outeish Taani Ds; An effective treatment for
chronic periodontal abscesses Quintessence
International Volume; 1996: 27, No. 10, Page 697699
[18]
Dimitroulis ; A synopsis of minor oral surgery;
1997: Reed education & Professional publication
Ltd. Chapter 8 (Odontogenic infections)
[19]
Mariano Sanz, David Herrera, and Arie J. van
Winkelhoff ;The Periodontal Abscess; page 496503;Jan Lindhe: Clinical Period ontology and
Implant Dentistry; 5th Edition
Fig 1: Periodontal abscess mesial to maxillary right
central incisor, copious pus exudate after pocket is
probed.
Fig 2: Radiogrph dipicts the periodontal probe inserted
the base of osseous defect
Fig 3: The periodontal abcsess mesial to maxillary right
first central incisor ha sopened through gingival
sulcus. Once the acute symptoms have subsided,
definitive treatment can be undertaken.
Fig 4: Radiograph 6 months after definitive therapy.
Some new bone formation is apparent.
17